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Gene expression clusters of a lipopolysaccharide‐stimulated pathway in peripheral blood monocytes of Japanese patients with Crohn's disease
Author(s) -
NAITO Y.,
TAKAGI T.,
MIZUSHIMA K.,
UETA M.,
KINOSHITA S.,
HANDA O.,
KOKURA S.,
ICHIKAWA H.,
YOSHIDA N.,
YOSHIKAWA T.
Publication year - 2006
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.2006.00054.x
Subject(s) - lipopolysaccharide , crohn's disease , tlr5 , innate immune system , immunology , medicine , stimulation , disease , gene expression , gene , immune system , biology , toll like receptor , genetics
Summary Background Recent reports support the notion that patients with Crohn's disease have a dysregulated innate immune response to endogenous flora. Aim To reveal the distinct gene expression clusters of a lipopolysaccharide‐stimulated pathway in the peripheral blood monocytes of Japanese patients with Crohn's disease. Materials and methods Total RNA was extracted from peripheral blood monocytes of four patients in the remission stage of Crohn's disease as well as four controls, and gene expression profiles before and after lipopolysaccharide stimulation were investigated using a high‐density oligonucleotide probe array. To focus on innate immunity, the expression of genes to be studied was narrowed down to 118 probe sets which were selected using the following keywords: lipopolysaccharide , toll , myd and tir along with a software of NetAffx Analysis Center. Results Using hierarchical clustering analysis, we picked up to 44 and 36 probe sets for which expression had decreased before and after lipopolysaccharide stimulation, respectively, in patients with Crohn's disease compared with healthy volunteers. The expression of TLR5, 7, MyD88, SIGIRR, and Tollip was decreased both before and after lipopolysaccharide stimulation in patients with Crohn's disease. Conclusion We found several interesting clusters in monocytes before and after stimulation with lipopolysaccharide. These genes may have been responsible for the immunological differences between the Crohn's disease and control patients.